Oxidative Stress-induced Mechanisms Research Articles

Evaluation of anti - diabetic activity of palmyrah (palm jaggery and palm honey) (Borassus flabellifer L.) against streptozotocin – nicotinamide induced diabetic wistar rats

Value-added products derived from Palmyrah (Borassus flabellifer L.), such as palm jaggery and palm honey, serve as alternative source of table sugar with a low glycemic index. During 2022–23, an experiment was to evaluate their anti-diabetic activity. The efficacy of palm jaggery and palm honey was assessed in diabetic rats at a dose of 200 mg/kg, and their effects were compared to those of oral glimepiride in a 28-days randomized control study. Biochemical estimations and histopathological analyses revealed that palm jaggery and palm honey possess anti-diabetic, antioxidant, anti-hyperglycemic, and insulinogenic properties. These Palmyrah products significantly enhanced insulin secretion by pancreatic ?-cells, leading to a marked reduction in blood glucose levels, serum uric acid, creatinine, and lipid peroxidise activity. Furthermore, the restoration of normal metabolic pathways reduced oxidative stress-induced mechanisms in diabetic rats treated with Palmyrah jaggery and honey. Hence, palm products could be used as an adjuvant in the treatment of diabetes mellitus.

Role of NAD+, Oxidative Stress, and Tryptophan Metabolism in Autism Spectrum Disorders

Autism spectrum disorder (ASD) is a pervasive neuro-developmental disorder characterized by impaired social interaction, reduced/absent verbal and non-verbal communication, and repetitive behavior during early childhood. The etiology of this developmental disorder is poorly understood, and no biomarkers have been identified. Identification of novel biochemical markers related to autism would be advantageous for earlier clinical diagnosis and intervention. Studies suggest that oxidative stress-induced mechanisms and reduced antioxidant defense, mitochondrial dysfunction, and impaired energy metabolism (NAD+, NADH, ATP, pyruvate, and lactate), are major causes of ASD. This review provides renewed insight regarding current autism research related to oxidative stress, mitochondrial dysfunction, and altered tryptophan metabolism in ASD.

Increased Markers of Oxidative Stress in Autistic Children of the Sultanate of Oman

Autism spectrum disorder (ASD) is a neurodevelopmental disorder of early childhood, and an enumeration about its etiology and consequences is still limited. Oxidative stress-induced mechanisms are believed to be the major cause for ASD. In this study 19 autistic and 19 age-matched normal Omani children were recruited to analyze their degree of redox status and a prewritten consent was obtained. Blood was withdrawn from subjects in heparin-coated tube, and plasma was separated. Plasma oxidative stress indicators such as nitric oxide (NO), malondialdehyde (MDA), protein carbonyl, and lactate to pyruvate ratio were quantified using commercially available kits. A significant elevation was observed in the levels of NO, MDA, protein carbonyl, and lactate to pyruvate ratio in the plasma of Omani autistic children as compared to their age-matched controls. These oxidative stress markers are strongly associated with major cellular injury and manifest severe mitochondrial dysfunction in autistic pathology. Our results also suggest that oxidative stress might be involved in the pathogenesis of ASD, and these parameters could be considered as diagnostic markers to ensure the prevalence of ASD in Omani children. However, the oxidative stress-induced molecular mechanisms in ASD should be studied in detail.

Mechanisms of Hop Inhibition Include the Transmembrane Redox Reaction

In this work, a novel mechanistic model of hop inhibition beyond the proton ionophore action toward (beer spoiling) bacteria was developed. Investigations were performed with model systems using cyclic voltammetry for the determination of redox processes/conditions in connection with growth challenges with hop-sensitive and -resistant Lactobacillus brevis strains in the presence of oxidants. Cyclic voltammetry identified a transmembrane redox reaction of hop compounds at low pH (common in beer) and in the presence of manganese (present in millimolar levels in lactic acid bacteria). The antibacterial action of hop compounds could be extended from the described proton ionophore activity, lowering the intracellular pH, to pronounced redox reactivity, causing cellular oxidative damage. Accordingly, a correlation between the resistance of L. brevis strains to a sole oxidant to their resistance to hop could not be expected and was not detected. However, in connection with our recent study concerning hop ionophore properties and the resistance of hop-sensitive and -tolerant L. brevis strains toward proton ionophores (J. Behr and R. F. Vogel, J. Agric. Food Chem. 57:6074-6081, 2009), we suggest that both ionophore and oxidant resistance are required for survival under hop stress conditions and confirmed this correlation according to the novel mechanistic model. In consequence, the expression of several published hop resistance mechanisms involved in manganese binding/transport and intracellular redox balance, as well as that of proteins involved in oxidative stress under "highly reducing" conditions (cf. anaerobic cultivation and "antioxidative" hop compounds in the growth medium), is now comprehensible. Accordingly, hop resistance as a multifactorial dynamic property at least implies distinct resistance levels against two different mechanisms of hop inhibition, namely, proton ionophore-induced and oxidative stress-induced mechanisms. Beyond this specific model of hop inhibition, these investigations provide general insight on the role of electrophysiology and ion homeostasis in bacterial stress responses to membrane-active drugs.

Os riscos e danos nas intoxicações por paraquat em animais domésticos

O paraquat é um herbicida de contato não-seletivo. É amplamente utilizado na agricultura em mais de 100 países, pois apresenta baixo custo, grande eficácia e não possui efeitos poluentes cumulativos para o solo. Porém, ele é um produto muito tóxico para humanos e animais, podendo causar intoxicações fatais, principalmente pela falta de um antídoto eficaz na reversão do quadro clínico. O paraquat atua mediante mecanismos de indução do estresse oxidativo, produção aumentada de radicais livres associada à depleção dos sistemas antioxidantes do organismo. Sua toxicidade acomete rins, fígado, músculos, cérebro, dentre outros. Os pulmões são considerados os órgãos-alvo deste herbicida, levando a severas injúrias como edema, hemorragia, inflamação intersticial e fibrose pulmonar. A falência respiratória grave é a causa comum de morte. O tratamento da intoxicação, atualmente, é baseado em medidas que diminuam a absorção e aumentem a excreção. Entretanto, o uso de agentes antioxidantes e antifibróticos vem sendo estudado, pois há interesse crescente no estudo de substâncias que possam servir como antídoto nas intoxicações, uma vez que o paraquat aumenta os índices de morbidade e mortalidade.

Free radical damage, iron, and Alzheimer's disease

We present evidence to support the premise that many of the pathological correlates of Alzheimer's disease are precipitated by free radical- and oxidative stress-induced mechanisms. We propose that amyloid-/3 deposition in senile plaques, intracellular accumulation of protein in neurofibrillary tangles, and the degeneration of specific neuronal populations can be attributed to specific oxidative stress-type mechanisms. Free radicals in disease pathogenesis, generated in part as a result of Fenton-type reactions, suggest that lowering the level of available iron, intervention with antioxidants, or the administration of free radical scavengers could provide a therapeutic inroad in the fight against Alzheimer's disease.